Insulin-like growth factor-1 and insulin-like growth factor binding proteins in cerebrospinal fluid during the development of mouse embryos

Salehi, Zivar; Mashayekhi, Farhad; Naji, Mohammad; Pandamooz, Sareh

doi:10.1016/j.jocn.2008.09.018

Cited by 32 publications

(31 citation statements)

References 25 publications

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“…Immunoblotting was carried out as described in a previous study [32] using antibodies against insulin-like growth factor 1 (IGF-1) (Santa Cruz, CA, USA) and Runt-related transcription factor 2 ( Runx-2 ) (Santa Cruz, CA, USA) with β-tubulin (Santa Cruz, CA, USA) used as loading control. Runx-2 and IGF-1 protein levels relative to β-actin protein amounts were assessed by densitometric analysis and expressed relative to the levels obtained for V-WT mice [33]. Bands were visualized using enhanced chemiluminescence (Amersham, Aylesbury, UK).…”

Section: Methodsmentioning

confidence: 99%

Exogenous PTHrP Repairs the Damaged Fracture Healing of PTHrP+/− Mice and Accelerates Fracture Healing of Wild Mice

Wang

Fang

Wang

et al. 2017

IJMS

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Bone fracture healing is a complicated physiological regenerative process initiated in response to injury and is similar to bone development. To demonstrate whether an exogenous supply of parathyroid hormone–related protein (PTHrP) helps in bone fracture healing, closed mid-diaphyseal femur fractures were created and stabilized with intramedullary pins in eight-week-old wild-type (WT) PTHrP+/+ and PTHrP+/− mice. After administering PTHrP for two weeks, callus tissue properties were analyzed at one, two, and four weeks post-fracture (PF) by various methods. Bone formation–related genes and protein expression levels were evaluated by real-time reverse transcriptase–polymerase chain reaction and Western blots. At two weeks PF, mineral density of callus, bony callus areas, mRNA levels of alkaline phosphatase (ALP), type I collagen, Runt-related transcription factor 2 (Runx-2), and protein levels of Runx-2 and insulin-like growth factor-1 decreased in PTHrP+/− mice compared with WT mice. At four weeks PF, total collagen-positive bony callus areas, osteoblast number, ALP-positive areas, and type I collagen-positive areas all decreased in PTHrP+/− mice. At both two and four weeks PF, tartrate-resistant acid phosphatase–positive osteoclast number and surface decreased a little in PTHrP+/− mice. The study indicates that exogenous PTHrP provided by subcutaneous injection could redress impaired bone fracture healing, leading to mutation of activated PTHrP by influencing callus areas, endochondral bone formation, osteoblastic bone formation, and bone turnover.

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Section: Methodsmentioning

confidence: 99%

Exogenous PTHrP Repairs the Damaged Fracture Healing of PTHrP+/− Mice and Accelerates Fracture Healing of Wild Mice

Wang

Fang

Wang

et al. 2017

IJMS

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“…The IGF1R and its ligands IGF-I and IGF-II are widely expressed in the developing CNS starting from early embryogenesis and continue to be expressed, with some variation in intensity, during CNS development and into adulthood; cells of all three neural lineages have been shown to express the IGF1R and secrete its ligands [56][57][58][59][60][61][62][63][64][65][66][67]. IGF-I, produced locally or delivered to the CNS from the circulation, induces a constitutive level of IGF1R-mediated signalling in the adult CNS, which is important for brain functions and adult neurogenesis [68].…”

Section: Igf1r In Neurogenesismentioning

confidence: 99%

The Insulin-Like Growth Factor (IGF) Receptor Type 1 (IGF1R) as an Essential Component of the Signalling Network Regulating Neurogenesis

Annenkov

2009

Mol Neurobiol

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The insulin-like growth factor receptor type 1 (IGF1R) signalling pathway is activated in the mammalian nervous system from early developmental stages. Its major effect on developing neural cells is to promote their growth and survival. This pathway can integrate its action with signalling pathways of growth and morphogenetic factors that induce cell fate specification and selective expansion of specified neural cell subsets. This suggests that during developmental and adult neurogenesis cellular responses to many signalling factors, including ligands of Notch, sonic hedgehog, fibroblast growth factor family members, ligands of the epidermal growth factor receptor, bone morphogenetic proteins and Wingless and Int-1, may be modified by co-activation of the IGF1R. Modulation of cell migration is another possible role that IGF1R activation may play in neurogenesis. Here, I briefly overview neurogenesis and discuss a role for IGF1R-mediated signalling in the developing and mature nervous system with emphasis on crosstalk between the signalling pathways of the IGF1R and other factors regulating neural cell development and migration. Studies on neural as well as on non-neural cells are highlighted because it may be interesting to test in neurogenic paradigms some of the models based on the information obtained in studies on non-neural cell types.

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“…IGFs primarily consist of the growth factors IGF-1 and IGF-2 and their corresponding receptors IGF1R and IGF2R, as well as IGF binding proteins (Jones and Clemmons, 1995). IGF-1 plays its role by acting on IGF1R and IGF2R through the MAPK pathway and the phosphatidylinositol 3-kinase (P13K/Akt) pathways (Salehi et al, 2009;Santen et al, 2009). BMPs are subject to the transforming growth factor-β superfamily.…”

Section: Discussionmentioning

confidence: 99%

Effect of Insulin-like Growth Factor-1 on Bone Morphogenetic Protein-2 Expression in Hepatic Carcinoma SMMC7721 Cells through the p38 MAPK Signaling Pathway

Cai²,

Wu³

2012

Asian Pacific Journal of Cancer Prevention

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Insulin-like growth factor-1 and insulin-like growth factor binding proteins in cerebrospinal fluid during the development of mouse embryos

Cited by 32 publications

References 25 publications

Exogenous PTHrP Repairs the Damaged Fracture Healing of PTHrP+/− Mice and Accelerates Fracture Healing of Wild Mice

Exogenous PTHrP Repairs the Damaged Fracture Healing of PTHrP+/− Mice and Accelerates Fracture Healing of Wild Mice

The Insulin-Like Growth Factor (IGF) Receptor Type 1 (IGF1R) as an Essential Component of the Signalling Network Regulating Neurogenesis

Effect of Insulin-like Growth Factor-1 on Bone Morphogenetic Protein-2 Expression in Hepatic Carcinoma SMMC7721 Cells through the p38 MAPK Signaling Pathway

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